Mannick has been exploring the effects of rapamycin-like drugs in covid-19. Her trial has been taking place in nursing homes experiencing outbreaks of the disease. For four weeks, half the participants were given the drug, while the other half were given a placebo. Among those given a placebo, “25% of them developed severe covid, and half of them died,” says Mannick, who has yet to publish the work. None of those taking the drug developed any covid-19 symptoms.
“There are multiple strategies of helping the aging immune system to fight against covid better,” she says. “Aging is the biggest risk factor for severe covid, and it’s a modifiable risk factor.”
She hopes to extend the use of her drug beyond covid-19; a rejuvenated immune system could theoretically fend off many other viral and bacterial infections. Her colleague Stanley Perlman, a coronavirologist at the University of Iowa who coauthored the research on BioAge’s covid drug in mice, has future pandemics in mind. “Next time there’s another coronavirus in 2030, maybe all this information will be very useful then,” he says.
Out with the old
The immune system isn’t the only target of anti-aging drugs. Others aim to clear out aged cells. Most of the cells in our body divide up to a certain point. Once they reach this limit, they should die and be cleared away by the immune system. But that’s not always the case—some cells linger on. These cells no longer divide, and some instead churn out a toxic brew of chemicals that trigger damaging inflammation in the surrounding area and beyond.
Cells that do this are called “senescent,” and they accumulate across our organs as we age. They’ve been linked to an ever-growing number of age-related diseases, including diabetes, heart disease, osteoporosis, cataracts, Alzheimer’s—the list goes on. They also appear to play an important role in coronavirus infections.
In yet-to-be-published research, James Kirkland, who studies aging and cell senescence at the Mayo Clinic in Rochester, Minnesota, says he has evidence that coronavirus more rapidly infects senescent cells than non-senescent cells. His research also suggests that senescent cells release chemicals that make neighboring non-senescent cells take up the virus too, he says.
Not only do these cells take on more coronavirus, but they also appear to provide a breeding ground for new virus variants. “There’s emerging evidence that senescent cells that are infected with coronavirus can mutate that virus,” says Kirkland. “So they may even be a cause of viral mutations.”
As an added concern, the coronavirus can make healthy cells senescent. Given all this, senescence has become an obvious target of both anti-aging and covid-19 therapies. Studies in mice and hamsters suggest that compounds that kill senescent cells can improve the symptoms of covid-19 and boost the chances of survival.